We propose the hypothesis that in many cases the damage to ocular tissues occurs during microbial infection, not from direct action of microbial products, but indirectly from activation of host enzymes by such products. Previous work has produced evidence for the role of pneumococcal cytolysin in the pathogenesis of corneal ulcers. Corroboration of this will be attempted by: (a) testing with corneal explants for activation of corneal degradative enzymes (e.g., collagenase) by the penumococcal cytolysin; and (b) isolation of, and assessment of pathogenicity of, non-hemoytic mutants. The role of cytolysins of Pseudomonas aeruginosa and Staphylococcus aureus will also be evaluated by production, isolation and purification of these agents, testing of their ability to produce corneal damage in vivo and performing corroborating experiments as described above for the pneumococcus. Further work will involve testing of agents (e.g., chelators) which might prevent these manifestations of pathogenicity by effecting inhibition, either at the level of the cytolysin, or of the corneal degradative enzymes.